Bacillus amyloliquefaciens SC06 Induced AKT–FOXO Signaling Pathway-Mediated Autophagy to Alleviate Oxidative Stress in IPEC-J2 Cells

Abstract

Autophagy is a conserved proteolytic mechanism, which degrades and recycles damaged organs and proteins in cells to resist external stress. Probiotics could induce autophagy; however, its underlying molecular mechanisms remain elusive. Our previous study has found that <i>BaSC06</i> could alleviate oxidative stress by inducing autophagy in rats. This research aimed to verify whether <i>Bacillus amyloliquefaciens SC06</i> can induce autophagy to alleviate oxidative stress in IPEC-J2 cells, as well as explore its mechanisms. IPEC-J2 cells were first pretreated with 10⁸ CFU/mL <i>BaSC06</i>, and then were induced to oxidative stress by the optimal dose of diquat. The results showed that <i>BaSC06</i> significantly triggered autophagy, indicated by the up-regulation of LC3 and Beclin1 along with downregulation of p62 in IPEC-J2 cells. Further analysis revealed that <i>BaSC06</i> inhibited the AKT-FOXO signaling pathway by inhibiting the expression of p-AKT and p-FOXO and inducing the expression of SIRT1, resulting in increasing the transcriptional activity of FOXO3 and gene expression of the ATG5-ATG12 complex to induce autophagy, which alleviated oxidative stress and apoptosis. Taken together, <i>BaSC06</i> can induce AKT-FOXO-mediated autophagy to alleviate oxidative stress-induced apoptosis and cell damage, thus providing novel theoretical support for probiotics in the prevention and treatment of oxidative damage.